NLK and neoplasm: Ji et al. have shown that forced expression of miR-181 enhances the tumor-initiating ability of EpCAM+ HCC cells by targeting hepatic differentiation regulators, such as caudal type homeobox 2 (CDX2), GATA binding protein 6 (GATA6), and nemo-like kinase (NLK, a Wnt/beta-catenin pathway inhibitor) [10].